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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Curr Opin Hematol. 2017 May;24(3):159–166. doi: 10.1097/MOH.0000000000000328

Figure 2. Pomalidomide and glucocorticoids are hypothesized to act on different erythroid progenitor populations.

Figure 2

(A) During steady-state erythropoiesis in the adult, the BFU-E population contains a small minority of HbF-producing cells (purple), and cells possess limited self-renewal. BFU-Es differentiate into CFU-Es followed by erythroid precursors and erythrocytes containing mainly adult hemoglobin (HbA). (B) Glucocorticoids appear to affect erythroid progenitors in a species-specific manner. In mice, glucocorticoids increase BFU-E self-renewal (green), whereas increased CFU-Es may result from glucocorticoid treatment in humans. The proportion of HbF-producing cells (purple) remains unchanged by glucocorticoid treatment. (C) Pomalidomide exerts its effect at BFU-E or on the BFU-E to CFU-E transition to induce HbF and increase BFU-E numbers through two potential mechanisms: (i) stimulate the expansion of pre-programmed HbF producing BFU-E (purple) or (ii) reprogram adult progenitors to prevent γ-globin repression (striped).